Left ventricular conduction delay due to bundle branch block causes regional heterogeneity in contraction and stretch, or asynchrony, which reduces pump function and stimulates negative left ventricular remodeling, such as increased chamber volumes. Experimental models have demonstrated a direct linkage between left ventricular electrical activation, cardiac mechanics, and remodeling. The conceptual basis of multisite pacing, which is also referred to as cardiac resynchronization therapy (“CRT”) or biventricular pacing, for asynchronous heart failure is to minimize ventricular conduction delay, which reduces contractile asynchrony and improves chamber mechanics. Resynchronization of electromechanical activation induces so-called “reverse” remodeling, characterized by ventricular volume reductions, and improved pump function, characterized by increased ventricular ejection fraction. Reverse remodeling is associated with reduced heart failure morbidity and mortality. However, up to one-third of patients do not improve following CRT.
The translational mechanism for reverse volumetric remodeling in response to multisite pacing for asynchronous heart failure is ventricular activation wavefront fusion, which is evident on the paced 12-lead surface ECG. Presence of ventricular activation wavefront fusion predicts increased probability of reverse remodeling, whereas absence of wavefront fusion predicts reduced probability of remodeling, regardless of baseline substrate conditions.
Unfavorable substrate conditions, such as high myocardial scar volume or small amounts of ventricular conduction delay, cannot be modified by pacing techniques. In contrast, pacing strategies can be readily adapted to modify ventricular activation, and such instructions can be implemented automatically in the fully ambulatory patient having a cardiac implantable electrical device (“CIED”). Recent experimental evidence indicates that only two-thirds of CIED patients have paced surface ECG evidence of ventricular activation wavefront fusion during conventional CRT. This implies that failure to correct ventricular conduction delay, despite conventional CRT pacing, contributes significantly to volumetric remodeling non-response.
The limitation of all existing CIED approaches to automatic or semi-automatic adjustment of pacing control systems for CRT is that they rely solely on limited device-based measurements that have not been correlated with improvement in any clinical outcome measure, most notably, reverse volumetric remodeling. It would therefore be desirable to provide a system and method for cardiac resynchronization therapy that more accurately characterizes global ventricular activation patterns and that results in clinically reliable measurements and changes to pacing control parameters.